Hemodynamic determinants of the time-course of fall in canine left ventricular pressure.

Weiss, James L.; Frederiksen, James W.; Weisfeldt, Myron L.

doi:10.1172/jci108522

Cited by 1,022 publications

(528 citation statements)

References 19 publications

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“…Isovolumic relaxation was measured by the logarithmic method of Weiss et al, T L (21) and the pressure half-time method of Mirsky, T 1/2 (22). Although there is no consensus as to the best mathematical estimate of the rate of isovolumic left ventricular relaxation, the methods used in this study have been advocated as reasonable indices of isovolumic relaxation (21,34,35). Despite reports that Tau is sensitive to changes in loading conditions (36), in the human left ventricle Tau has been shown to be insensitive to relatively small changes in load (34,35).…”

Section: Discussionmentioning

confidence: 98%

“…The time constant of left ventricular relaxation, Tau, was calculated in two different ways. The first method is a modification of that described by Weiss et al, such that Tau (T L ) ϭ Ϫ 1/slope of the regression line for the natural logarithm of left ventricular pressure versus time for the period from peak Ϫ dP/dt to 5 mm Hg above left ventricular end-diastolic pressure (21). The second method is the direct measurement of the pressure halftime (T 1/2 ), as described by Mirsky (22).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Muscarinic receptor modulation of basal and beta-adrenergic stimulated function of the failing human left ventricle.

Newton¹,

Parker²,

Landzberg³

et al. 1996

J. Clin. Invest.

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The objective of this study was to evaluate the effect of muscarinic receptor modulation on basal and ␤ -adrenergic stimulated left ventricular function in patients with heart failure. 21 heart failure patients and 14 subjects with normal ventricular function were studied. In Protocol 1 intracoronary acetylcholine resulted in a 60 Ϯ 8% inhibition of the left ventricular ϩ dP/dt response to intracoronary dobutamine in the normal group, and a similar 70 Ϯ 13% inhibition in the heart failure group. Acetylcholine also attenuated the dobutamine-mediated acceleration of isovolumic relaxation (Tau) in both groups. Acetylcholine alone had no effect on Tau in the normal group, while it prolonged Tau in the heart failure group. In Protocol 2 intracoronary atropine resulted in a 35 Ϯ 10% augmentation of the inotropic response to dobutamine in the normal group, versus a non-significant 12 Ϯ 15% augmentation of the dobutamine response in the heart failure group. In Protocol 3, in 6 heart failure patients, both effects of acetylcholine, the slowing of ventricular relaxation and the inhibition of ␤ -adrenergic responses, were reversed by the addition of atropine. Therefore, in the failing human left ventricle muscarinic stimulation has an independent negative lusitropic effect and antagonizes the effects of ␤ -adrenergic stimulation. ( J. Clin. Invest. 1996. 98:2756-2763.)

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Section: Discussionmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

Muscarinic receptor modulation of basal and beta-adrenergic stimulated function of the failing human left ventricle.

Newton¹,

Parker²,

Landzberg³

et al. 1996

J. Clin. Invest.

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show abstract

“…Peak negative dP/dt and t, both of which are indices of LV relaxation, 19,23,29 were significantly impaired in the HT, DM and HT+DM groups as compared with those in the control group, and this impairment was significantly exaggerated in the HT+DM group than in the HT group in terms of t (Table 1). Although the LV end-diastolic pressure was within the normal range in all groups, it was significantly higher in the HT and HT+DM groups than in the control group ( Table 1).…”

Section: Hemodynamicsmentioning

confidence: 96%

Diabetes mellitus accelerates left ventricular diastolic dysfunction through activation of the renin–angiotensin system in hypertensive rats

et al. 2009

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Diabetes mellitus (DM) is a major risk factor for heart failure, independent of coronary artery disease or hypertension (HT). Therefore, our study was designed to examine the mechanisms of DM-induced left ventricular (LV) diastolic dysfunction. In this study, we made five different 10-week treatment groups of Dahl salt-sensitive rats as follows: Control; a low-salt (0.5% NaCl) diet, HT; a high-salt (5% NaCl) diet, DM; a low-salt diet with streptozotocin (STZ) injection (30 mg kg À1 i.p.), HT+DM; a highsalt diet with STZ injection, and the Olmesartan group; a high-salt diet with STZ treated with an angiotensin receptor blocker, olmesartan (1 mg kg À1 day À1 ). Cardiac diastolic dysfunction with a preserved systolic function was noted in the HT group, and was most prominently noted in the HT+DM group, characterized by enhanced cardiac fibrosis, whereas the extent of HT and myocardial hypertrophy was comparable between the two groups. Myocardial expressions of collagen III, transforming growth factor-b2, angiotensin-converting enzyme (ACE), angiotensin II type-1 receptor and myocardial oxidative stress (evaluated by 4-hydroxy-2-nonenal-modified protein) were mostly enhanced in the HT+DM group. Importantly, there was a positive correlation between the extent of diastolic dysfunction and that of myocardial ACE expression. All these cardiac abnormalities induced by DM and HT were ameliorated in the olmesartan group. These results indicate that DM accelerates diastolic dysfunction in hypertensive heart disease through activation of the renin-angiotensin system, with subsequent inflammatory and oxidative stresses and myocardial fibrosis, suggesting that an inhibition of the system is effective for the treatment of diastolic dysfunction in this combined disorder.

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“…Effective arterial elastance (Ea) to assess afterload was also assessed. The diastolic parameters of ventricular function were end‐diastolic pressure (EDP), the maximum rate of isovolumic relaxation (dP/dt min ), and the time constant of diastolic relaxation (Tau) 22, 23, 24. Tau represents the exponential decay of the RV pressure during isovolumic relaxation.…”

Section: Methodsmentioning

confidence: 99%

“…Tau represents the exponential decay of the RV pressure during isovolumic relaxation. Tau was determined using the Weiss method 22. Tau was calculated as a parameter in an exponential fit using the following equation: P(t)=A exp (−t/Tau).…”

Section: Methodsmentioning

confidence: 99%

Stunning and Right Ventricular Dysfunction Is Induced by Coronary Balloon Occlusion and Rapid Pacing in Humans: Insights From Right Ventricular Conductance Catheter Studies

Axell

Giblett

White

et al. 2017

JAHA

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BackgroundWe sought to determine whether right ventricular stunning could be detected after supply (during coronary balloon occlusion [BO]) and supply/demand ischemia (induced by rapid pacing [RP] during transcatheter aortic valve replacement) in humans.Methods and ResultsTen subjects with single‐vessel right coronary artery disease undergoing percutaneous coronary intervention with normal ventricular function were studied in the BO group. Ten subjects undergoing transfemoral transcatheter aortic valve replacement were studied in the RP group. In both, a conductance catheter was placed into the right ventricle, and pressure volume loops were recorded at baseline and for intervals over 15 minutes after a low‐pressure BO for 1 minute or a cumulative duration of RP for up to 1 minute. Ischemia‐induced diastolic dysfunction was seen 1 minute after RP (end‐diastolic pressure [mm Hg]: 8.1±4.2 versus 12.1±4.1, P<0.001) and BO (end‐diastolic pressure [mm Hg]: 8.1±4.0 versus 8.7±4.0, P=0.03). Impairment of systolic and diastolic function after BO remained at 15‐minutes recovery (ejection fraction [%]: 55.7±9.0 versus 47.8±6.3, P<0.01; end‐diastolic pressure [mm Hg]: 8.1±4.0 versus 9.2±3.9, P<0.01). Persistent diastolic dysfunction was also evident in the RP group at 15‐minutes recovery (end‐diastolic pressure [mm Hg]: 8.1±4.1 versus 9.9±4.4, P=0.03) and there was also sustained impairment of load‐independent indices of systolic function at 15 minutes after RP (end‐systolic elastance and ventriculo‐arterial coupling [mm Hg/mL]: 1.25±0.31 versus 0.85±0.43, P<0.01).ConclusionsRP and right coronary artery balloon occlusion both cause ischemic right ventricular dysfunction with stunning observed later during the procedure. This may have intraoperative implications in patients without right ventricular functional reserve.

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Hemodynamic determinants of the time-course of fall in canine left ventricular pressure.

Cited by 1,022 publications

References 19 publications

Muscarinic receptor modulation of basal and beta-adrenergic stimulated function of the failing human left ventricle.

Muscarinic receptor modulation of basal and beta-adrenergic stimulated function of the failing human left ventricle.

Diabetes mellitus accelerates left ventricular diastolic dysfunction through activation of the renin–angiotensin system in hypertensive rats

Stunning and Right Ventricular Dysfunction Is Induced by Coronary Balloon Occlusion and Rapid Pacing in Humans: Insights From Right Ventricular Conductance Catheter Studies

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